Aside from the well-recognised effects on the the lungs, COVID-19 infection can affect the heart in a number of ways. Firstly, COVID-19 can make the blood more sticky leading to blood clots. This, combined with oxygen deprivation can cause a heart attack, which is where part of the heart becomes deprived of an adequate blood supply and dies off. However, it would appear that the virus can affect the heart directly, causing heart muscle damage. This can lead to heart rhythm problems and heart failure. When COVID affects the heart in this way, it is termed myocarditis. Damage to the heart at the time of COVID-19 infection is associated with a higher death rate. Many viruses can do this, and this one is no exception. The type of damage that has occurred can be determined by MRI scanning.
It may be more common than is widely appreciated. COVID-19 infection is still a new infection and we are still at the early stages of understanding it. Although many people appear to have no or few symptoms, it’s clear that some people are severely affected and that some people have symptoms that persist for some time after infection.
After having had COVID-infection, assuming your symptoms have not been too bad, once recovered it would be wise to wait a week to 10 days before resuming athletic activity. It is then a case of listening carefully to your body and easing back into things. It may take a bit longer before you feel completely back to normal.
If you have had a more severe infection then you may go on to experience extreme fatigue, breathlessness and fast heart rates which can persist for some time. This “long-Covid” is poorly understood and may point towards more significant damage. In this case, it is probably wise to avoid sporting activity and seek further medical evaluation. We need to emphasise that we are in the very early stages of understanding this disease. Therefore, be aware that the advice may change frequently as more and more is found out.
Firstly, a tragic death in London this weekend, widely covered in the press. It will likely be either hyponatraemia (too much fluid and too little salt) or heat stroke, given his age. Time will tell.
One of the other questions was whether or not someone would run Sub-2. The answer was no. Firstly because it was too hot. And secondly because the data said not. It’s not likely to be before 2030 at the rate it is going. I haven’t plotted a 95% CI, but perhaps with a few more technical and training examples, some competition, and optimal conditions, it may be sooner.
See what you think. I have updated some charts I have with the 2018 finish times. I won’t be reading articles about Sub-2 times in London for a while, but on a track in Italy, maybe…
The other week one of our Crickles members recorded something odd. He was cycling on Zwift (Zwift Fondo Wk1 Wo2), and is a keen cyclist, typically putting in 3-4 sessions per week. It’s ideal for the time-crunched, particularly over winter.
He had been noticing something odd for a while, but he and his doctor had dismissed the symptoms. He would notice that his heart had gone “mad” and that he had to slow down or sometime stop. The symptoms would last for 10 minutes at most. He could then carry on.
In recent months he has been wearing a heart rate chest strap more regularly, but still sporadically, and then this happened:
There was a sudden jump in his heart rate. Most importantly he felt odd with it too. It came at the end of the ride. The heart rate was out of kilter with his power output. It wasn’t “geometric” – that is there was variability in the heart rate. It fell slightly as his power output fell. Naturally he finished the ride.
For all of these reasons, it looked like a genuine heart rhythm problem. So, he got an AliveCor. This is a small device which pairs with a smartphone or tablet and can record a single lead electrocardiogram. You can buy them from the manufacturer, or Amazon.
A few days later, whilst running, his heart rate jumped again, and this time he caught it on the AliveCor:
This shows a supraventricular tachycardia, with a heart rate of 220bpm or so. It’s just gone back to normal at the end of the trace. Although you can’t quite see a “QRS” complex (a sign that the bottom part of the heart, the ventricle, has activated), you can see a pause and a “p wave” (a sign that the top part of the heart, the atrium, has activated).
This is a common, not life-threatening, rhythm problem. Most people have a single connection between the atria (at the top) and the ventricles (at the bottom, the pumping chambers of the heart). Some people have two (or more), and then, under certain circumstances, the electrical signals can pass down one of the connections and back up the other, looping round in a small circuit and stimulating the heart to go quickly. This is technically known as an atrio-ventricular (nodal – if the pathways are in a structure called the atrio-ventricular node) re-entrant tachycardia. In this case, it’s most likely that both connections in the node.
The definitive treatment is an electrophysiology study and ablation. This maps out the pathways and burns or freezes one of them. It has a good success rate, and is usually curative (about 90-95%), and a low (but not zero) complication rate.
He is on the list for this procedure (thanks Graham!), and in the meantime is on a drug called flecainide, as he will have to wait a little while. The drug is working. But drugs aren’t ideal when there is a procedure that can cure the situation.
The irony is that it’s my son. I never thought that when we started this project, the work would help me directly.
Good luck to those running the marathon today. I’m out for a ride. With my son. It will be his longest to date at 100K. I’ll be honest to say I am a little nervous.
I am sure many of you will have seen the tragic footage by now. He was dead on the bike. He came around the corner and went straight on into the bank with no effort to protect himself or steer. It was shocking.
There was this statement, widely reproduced:
“The autopsy confirms the previous hypothesis that death was due to a heart attack and not a crash. He suffered an attack while racing. His heart stopped, and that’s why he crashed”
Remy Schwartz, the state prosecutor for Cambrai
The slight issue I have is with the word heart attack. A heart attack is a specific term for when a blood vessel in the heart becomes blocked and part of the heart muscle dies. This can result in death. Heart attacks are possible, but vanishingly rare. He could have dissected a coronary artery – that is where an artery splits. He could have a coronary artery anomaly – that is where an artery takes an unusual course in the body and can get compressed during extreme exertion. Finally he could have typical coronary artery disease, but the chances of someone like him having typical coronary artery disease (which normally takes decades of smoking, diabetes and high cholesterol levels to provoke) must be vanishingly rare.
What is more likely is that they meant heart arrhythmia – that is the heart beating too quickly – ventricular tachycardia or fibrillation. It is common to call a cardiac arrest (where the heart stops pumping blood effectively) a heart attack, and the two are very different. Let’s see what further tests show.
I guess what has shocked me the most is how most coverage focused still on Sagan (who, to be fair, rode amazingly), and how the world moved on to the Amstel Gold race. I don’t think that life will have moved that quickly for his family, friends and team-mates.
I was going to write about something else this weekend. But then I read that Michael Goolaerts had a cardiac arrest at Paris-Roubaix.
He reportedly had a cardiac arrest after a crash and received CPR at the roadside.
We don’t know much more at the time of writing.
He may have simply crashed and struck his chest. He was on the cobbles at the time, and they are notorious. Commotio Cordis is the term given when a blow to the chest wall put the heart into ventricular fibrillation. It’s most common in boys/young men when they are playing sport. It’s more common than you might think. According to Wikipedia there were 188 cases in the US between 1996 and 2007. 4 in 5 died.
There are a few conditions which he might have had. I thought that cycling at this level would require a basic history, exam, electrocardiogram (which looks at the electrical system) and echocardiogram (echo). An echo is not necessary it would seem (see here). Echocardiography looks at the structure of the heart and is a very common test that is requested on most patients a cardiologist would see. If I was competing at such a level (which I never will) I would want one. Therefore the medical exam has to be considered as pretty cursory.
Nonetheless, the screening as it is might be expected to exclude conditions such as hypertrophic cardiomyopathy (the muscle layers of the heart become disorganised), possibly arrhythmogenic right ventricular dysplasia (fat replaces muscle in the heart), and significant valve disease such as aortic stenosis (blood can’t get out of the heart properly). These are structural problems with the heart which can result in sudden death. Problems with the electrical system such as long QT syndrome or Brugada syndrome (these can predispose people to abnormal life threatening heart rhythm problems) could also be picked up.
Aside from an echo, an exercise ECG might help too – that is an ECG recorded during (and shortly after) exercise. One of the most common causes of death during exercise in young people are aberrant coronary arteries. The coronary arteries supply the heart with blood. Sometimes they take odd paths through the body. There is one route which they sometimes take when one of the runs between the aorta (the tube that takes blood from the heart around the body) and the pulmonary artery (the tube that takes blood from the heart to the lungs). At times of physical stress the coronary artery can become compressed and blood can’t get to the heart, resulting in cardiac arrest. You can see the early stages of that on an exercise test.
There is always the spectre of drug use too. I hate to say it, and I hate to think it, but I am still suspicious of what goes on in professional cycling (and other sports).
Sadly the outlook from “out-of-hospital”, and indeed “in-hospital” cardiac arrest is still poor. But I hope he will be ok. He will have been spotted quickly and had good cardiopulmonary resuscitation early, which will improve his chances. He’s also young and fit, which again stands in his favour. Fingers crossed.
I have been in the 48:30s for my 10Ks so far. Mo Farah can sleep soundly in his bed. My fastest 10K, according to Strava, came during the Bristol Half Marathon last year (surprisingly). On Tuesday night, in my Nike’s I ran 46:31. About 2 minutes faster. So the shoes are better in the real world too. Frustratingly I can’t remember my previous best – and Strava doesn’t give you a list for some unknown reason.
Looking back at some of the segments I have run repeatedly during the route, I was a few percent faster consistently. What really surprised me was that I had done a run in the morning, and an hour and a half on the turbo too, doing intervals, so I was far from rested.
The shoes are not going back. I’m amazed. If you buy a TT bike and a speed suit and a helmet, and spend time in the wind tunnel, you expect some time back “for free”. But I had never expected that shoes could make so much difference to running.
Last May I was struggling with lateral knee pain. For days after the Taunton half marathon I couldn’t walk down stairs. I had tried a few things and was about to spend a lot on a trip to a podiatrist. Instead I went to TriUK in Yeovil and had a go at their “Mizuno Running Solution”. They picked out some shoes for me and I haven’t looked back – I haven’t had knee pain since (I have had Achilles discomfort, lateral foot pain and posterior tibial tendonitis mind you – but nothing terrible). I’m on my third pair of Mizuno’s now. My wife and kids have pairs too.
I have been using the Wave Mujin 3 shoes over the winter. They have taken me through umpteen muddy fields and down paths as well as covered a lot of road miles. I have probably done 400-500Km in them. They have been through the washing machine umpteen times (I know…).
I thought it was time for some new shoes. The Nike app texted me last week to say that their new lightweight Epic React Flyknits were available. 5 minutes later I had ordered a pair and they arrived last Wednesday. They have a new type of foam in (“React”). It’s durable and returns energy to the runner. It’s no Zoom Vaporfly 4%, with no carbon fibre plate (as far as I know). But it’s not exorbitantly expensive and the shoes expected to be durable – 600 miles or so.
On Friday I took them for a spin. On a treadmill. My “fast” mile felt easier than ever – rather than feeling as though I was going to pass out at the end of it, I was increasing the speed and went on for 2Km.
Psychological? Possibly. I firmly believe in psychology. I have a degree in it, and my PhD was on “central fatigue” – the concept that your brain limits your exercise capacity. I spent a lot of time doing transcranial magnetic stimulation. It’s odd to see the resurgence recently in brain stimulation. There is no doubt that new kit gives you a boost. But certain parameters, such as heart rate don’t (shouldn’t) lie.
Last night I settled down for some science. I’ll need to replicate this again, probably next Sunday, but the bottom line is that the new shoes seem faster.
Some methods. I warmed up outside with a 3K run up and down our local hill. I then did 5 intervals on our treadmill: 800m at 11.3Km/h then 800m at 16.2Km/h then a brief rest (I let the treadmill run at 9Km/h for 400m – 160s). A total of 8K. That rest time allowed me to slow down, get off the treadmill and change my shoes and my footpod (Polar). I used a Polar H10 heart rate strap and recorded it on my Garmin 935. The first interval was with the Mizuno shoes. Then two intervals with the Nike’s. Then an interval with the Mizuno’s and then a final interval with the Nike’s. For reference I weighed the shoes – a single Nike weighs 234g, a single Mizuno weighs 388g – an important difference.
Note I can run “faster” on the treadmill than in real life. I have just managed a Sub 20 5K on the treadmill, but it’s still just over (by about 40s) on the local 5K park run. 11.3Km/h is the speed I target for endurance. Last year that kept my heart rate about 130-135bpm. 16.2Km/h is the fastest I can sustain for a mile. Because I wanted to see if the new shoes were faster I didn’t want to hit my maximum heart rate and plateau, so although I can go a (little) bit faster over 800m I kept it at this level.
What did it show?
Firstly, it felt way easier with the Nike’s. There is a definite squish and you can feel the shoe deforming on impact with your toes and forefoot sinking into the shoe. You don’t get that with the Mizunos. But was it physiologically easier?
It looks like it was. See figure 1. It has two traces on it. There is an actual speed (according to the treadmill) line to demonstrate the intervals and a heart rate trace. The orange intervals are when I have the Mizuno’s on. The Black intervals are when I have the Nike’s on.
Firstly, from left to right there is a gradual increase in heart rate. For me, running the 5 back to back intervals was hard. I’m also in a small, hot stuffy room. So I get tired and dehydrated.
But the interesting thing for me is that my peak heart rate is higher on interval 4 than interval 5, by just over 4 beats per minute. The trend would suggest it should be the other way around. Not much – but around 3%.
The really interesting thing is the speed data from the footpod though. The next chart (figure 2) shows the actual speed (calibrated – the actual data suggested I was much faster than I was!). As far as the footpod was concerned I was running more slowly (about 2Km/h) with the Nike’s on compared with the Mizuno’s, although the treadmill speed was the same.
I’m not quite sure why this is. Running in the Nike’s changed my technique though. I felt a bit more tipped forward and a bit more on my toes. I also noticed a bounce, and I would imagine I spent more time in the air, allowing the treadmill to travel further beneath me.
I have summarised the data in the table (table 1). I can go faster on the treadmill in the Nike’s. But am I faster in real life? I’ll try to answer that soon. As soon as the weather dries up anyway and I have some time to do some intervals outside. I don’t want to get my Nike’s dirty yet, and time is a bit tight at the moment. I also need to do a long run first to see if they are comfortable enough. The toe box is a bit small, and I don’t know how my knee will stand up to things. If I can’t get on with them, back they will go. Despite the treadmill times.
This morning I ran up Quakinghouse lane with the dogs and one of my kids. For about the first time in a while I enjoyed it. At the top of the hill the sun was rising, the wind had dropped, and I could see out over the vale of Taunton. There was a chance I would get home with warm, dry feet.
It’s been a long hard winter, and running up and down that hill hasn’t been pleasurable. But people who run (or cycle) are addicted to running (or cycling), and I am now a slave to it. And it is an addiction.
There is a long-running study looking at Ultra marathoners (the ULTRA study). It takes a little finding. There is a study on the treatment of fibroids known as Ultra, and project MKUltra is also known as the CIA mind control program – allegedly.
The signup for the study is here if you are interested. It’s an ambitious project to determine whether running long distances is healthy. If you are one of the many who has done an Ultra, then go and sign up.
But the interesting thing about people who do Ultras (people can enrol in the study if they have run an event of more than 50K) is that they don’t care if it’s healthy or not. Participants in the study were asked to answer “yes” or “no” to the question “If you were to learn, with absolute certainty, that ultramarathon running is bad for your health, would you stop your ultramarathon training and participation?” Of 1349 who answered the question, almost ¾ answered “no”. My guess is that this would hold true for cyclists and triathletes too. The Pubmed link is here if you want to read a bit more.
I see people with heart trouble every day of the week, that may be due to exercise. I haven’t stopped yet and won’t for as long as my health and my joints can keep going.
It absolutely p****d down as I ran down Quakinghouse lane. The shoes are on the Aga. I’ll be out again tomorrow.
It’s been one of those weekends which haven’t been full of joy. At one stage yesterday, with the rain pouring and the wind blowing, I asked myself what I was doing out running up a muddy hill with the dogs. The answer was of course to take my mind of the Bawa-Garba case.
For those of you who don’t know, Dr Bawa-Garba was found guilty of manslaughter and struck off by the GMC after the tragic death of a child under her care. She made a mistake – that is clear – and it had terrible consequences. But there were, as there usually are with mistakes, also problems with the system in which she worked. She had just returned from maternity leave, was working in an unfamiliar environment, the IT system was playing up and she had with junior doctors supporting her with little experience. It has been reported that she was covering for absent colleagues, including the consultant as well. Is it any wonder that a mistake happened?
This winter in the NHS has left many of us rushing around, managing a much higher number of patients than usual, and consequently making hurried judgements. But what is the alternative – to say you will only see a certain number of patients, or down tools if members of the team are off with flu? The case has made many of us feel vulnerable. All doctors make errors at times. We know we make more errors when under pressure.
The practice of medicine relies on judgement and intuition – which is why it is error prone. It is not an exact science, and never will be.
It is that very lack of hard data that inspired Crickles. I was asked “how much exercise is too much”, and I couldn’t give an exact answer. Crickles draws on the wisdom of the crowds. You can look at your exercise volume and see where you are relative to others. You can look at your fitness and fatigue levels. As of this evening, I am fatigued according to my data. So, it’s a day off training tomorrow, thank God, as the weather looks crap.
Shortly after writing my previous post, suggesting Tour de France riders live longer than normal people, I came across another study published in the British Journal of Sports Medicine. It was entitled “Mortality and health-related habits in 900 Finnish former elite athletes and their brothers”. The link is here.
They looked at male Finnish elite athletes who represented Finland between 1920 and 1965 and their age-matched brothers (not identical twin brothers necessarily). Fortunately having brothers seems common in Finland where it is often dark and cold.
They followed them from the start of their career up to 31st December 2015. 1296 of the 1800 died during the study period. The median age at death was as follows:
Elite athletes smoked less and were more physically active in general. We don’t know why elite athletes live longer, but their overall lifestyle, which includes exercise, seems to be protective.
This is an observational study, and not an experiment. It remains possible that the difference in smoking rates or some other lifestyle factors made the difference, and the excess exercise narrowed the gap – the study does not exclude the possibility that exercise is harmful in excess. It also doesn’t tell you that endurance sports make you live longer than power sports – just that those that tended to do endurance sports came from families that tended to live longer.
But I’m still doing some triathlons this year. And I will still be advising my patients to exercise. I’ll dig out the paper, hopefully, and see if there are any more details buried within it that are important.